During fiscal year 2011, our goal was to rigorously demonstrate that either Pim2 kinase or mTOR activity were signaling intermediates for p100 (NF&#954;B1) production by tonic BCR signaling. This required us to analyze p100 production in Pim2-deficient B cell treated with rapamycin. However, our efforts were hindered by the non-availability of Pim2-deficient mice from our collaborators at University of Massachusetts Medical Center. Additionally, we examined Mcl-1 expression in response to tonic, or acute, BCR signaling. We found that loss of Mcl-1 protein was accentuated in splenic B cells, treated with a PI3 kinase exhibitor (in the absence of BAFF). These observations suggest that tonic BCR signaling maintains Mcl-1 expression via PI3K. Since BAFF/BAFF-R interactions have also been shown to activate PI3K, Mcl-1 expression may be jointly regulated by BCR- and BAFF-R-initiated PI3K activation.